The mechanical effects of the muscle pump and arterial vasodilation are thought to be two important determinants of exercise hyperemia. The contributions of either to exercise hyperemia in humans are not clear. In addition, the possible interactions of chemically induced dilation (e.g. metabolites) and mechanical factors in determining exercise hyperemia have not been determined. The proposed experiments are designed to determine 1) whether increasing resting forearm blood flow alters the hyperemic response to a single mechanical compression or voluntary contraction, 2) whether increasing resting forearm blood flow alters the hyperemic responses to steady state exercise or rhythmic mechanical compression, and 3) whether endothelium-derived vasodilators contribute to the hyperemic response of a single muscle contraction or mechanical compression. This unique approach will measure forearm hyperemia to compression or contraction at three different levels of "resting" blood flow. Most studies of exercise hyperemia focus on the contribution of a single factor, rather than how mechanisms interact. The strength of the proposed experiments is that we will manipulate both mechanical and chemical factors and assess their combined effects on muscle blood flow during acute and steady state exercise in humans.